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A brief overview of crystalline silica
FEATURE
A brief overview of crystalline silica Silicon, and its oxide silica, are naturally abundant. Exposure to crystalline silica has long been known to cause silicosis and other lung disorders. Crystalline silica exposures are also associated with development of active tuberculosis, lung cancer, and certain autoimmune and renal disorders. Silicosis may occur in acute, accelerated and chronic forms with latency periods ranging from weeks to 40+ years, respectively. Silica exposure is controlled by the same methods that apply to any other dust inhalation hazard. No specific OSHA standard applies, beyond the PELs published in 29 CFR. These PELs depend on determination of the percent silica in a sample. This analysis should be performed in accordance with NIOSH analytical methods.
By Eileen Mason, Sophie K. Thompson
INTRODUCTION
Silicon is the second-most abundant element in the world.1 Silica, the common oxide, (SiO2) occurs naturally and is widespread. Crystalline forms of silica include alpha- and beta-quartz, cristobalite and tridymite. Because, alphaquartz is the most thermodynamically stable form, most naturally occurring crystalline silica is found in this morphology.2 Alpha-quartz has the greatest health impact because it is encountered most often. Cristobalite and tridymite are formed by exposure to high temperature, such as volcanic processes, or by calcining diatomaceous earth. Tridymite tends to be less hazardous than other crystalline forms, and amorphous silica is of lesser toxicological interest than crystalline silica. Because silica, especially in the form of quartz, is so ubiquitous, exposures may occur in any dusty location, and Eileen Mason is affiliated with Murray State University, Occupational Safety & Health, 157 IT Center, Murray, KY 420071, United States (e-mail: [email protected]). Sophie K. Thompson is affiliated with Old Dominion University, United States (e-mail: [email protected]).
6
may be both occupational and nonoccupational. Common beach sand is almost pure silica, as is volcanic glass. Topsoil, dust, and sedimentary and metamorphic rocks all contain silica in varying amounts. Granites contain in the neighborhood of 30% quartz, while shales are comprised of about 20% quartz. Some igneous rock may contain silica. Diatoms and radiolarians extract silica from water to form shells. Deposits of these shells are mined as diatomaceous earth, a noncrystalline form of silica. Opal, perlite and pumice are composed of amorphous hydrated silica. Historical Background
Reports of adverse health effects of exposure to silica date back to the ancient Greeks.3 Agricola’s 1556 Treatise on Mining describes pulmonary effects of silica exposure, and the topic is again discussed by Ramazzini in 1713. Today, we realize that it is primarily the crystalline form of silica that presents the health hazard. Such information was not available historically. Silicosis, a type of pneumoconiosis, occurs when crystalline silica particles are deposited in the lung tissue, leading to fibrotic changes. This accumulation of crystalline silica dust in the lungs has been known historically as ‘‘miners’ asthma’’, ‘‘potters rot’’, ‘‘phthisis’’, ‘‘stonemason’s disease’’ and ‘‘sewer disease’’.4 By the 1920s, dust inhalation, especially in the granite industry, was recognized as a serious health problem.
ß Division of Chemical Health and Safety of the American Chemical Society Elsevier Inc. All rights reserved.
During the 1930s, after the Hawks Nest disaster gained national attention, silicosis was considered the most serious occupational disease in this country. The Hawks Nest disaster occurred during the period 1930– 1931, when approximately 5,000 workers were employed to bore a tunnel through Gauley Mountain in West Virginia.5 About half of these employees worked inside the tunnel, excavating sandstone which was estimated to contain over 90% silica. Respiratory protection was supplied only to management, and wet drilling methods were used infrequently, since dry drilling was faster. A historical marker on the site documents a total of 109 deaths, but subsequent studies determined that at least 764 workers died due to silicosis and other silica-related conditions. At this time, safety laws were promulgated at the state level. Although only 11 states regulated silica exposure prior to Hawks Nest, congressional hearings held in 1937 were followed by passage of laws in an additional 35 states.
TOXICOLOGY
Silicosis may be acute, chronic, or accelerated. In all its forms, silicosis is incurable and symptoms are difficult to manage. The disease may progress even if there is no further exposure to silica. Inevitably, silicosis leads to serious loss of function and often death.
1871-5532/$36.00 doi:10.1016/j.jchas.2009.09.001
Overwhelming exposure to silica results in acute silicosis. Symptoms may become apparent within a few weeks. Employees at the Hawks Nest project were hired for periods averaging only 15 weeks – so that they could ‘‘leave the area and die someplace far from the source of their illness’’.6 Although relatively rare, acute silicosis still occurs among sandblasters and silica flour mill employees.7 Acute silicosis seems to involve an immune mechanism distinct from those associated with chronic and accelerated silicosis. Chronic silicosis, also known as silico-proteinosis or alveolar lipoproteinosis-like silicosis, is the most common presentation and typically appears 20– 40 years after initial exposure. Symptoms may be mild or absent for extended periods, with subsequent development of a dry cough and shortness of breath during exertion. Eventually, the cough becomes persistent and productive, with shortness of breath during normal activity. Examination of chest X-rays shows development of characteristic, extremely hard silica nodules, primarily located in the mid- and upper zones of the lung. These nodules proliferate and may coalesce as the disease progresses to massive pulmonary fibrosis. Eventually, pneumothorax and respiratory failure result. Accelerated silicosis is similar to chronic silicosis, but the latency period is reduced to 5–15 years from initial exposure, and the disease progresses more rapidly than does chronic silicosis. Exposure to crystalline silica is associated with a variety of respiratory diseases in addition to silicosis. There is a clear association between silica exposure and development of active tuberculosis, not only among silicotic individuals, but even in those who have long-term exposure to silica dust but do not have silicosis. Epidemiological studies have also shown an association between silica exposure and chronic bronchitis, emphysema and other forms of chronic obstructive pulmonary disease. Initial reports from Sweden8 and Ontario9 and additional studies during the 1980s confirmed a probable relationship between crystalline silica and
lung cancer. In 1987, IARC classified crystalline silica as Group 2A, Probably Carcinogenic to Humans.10 In 1996, with additional information, IARC revised the classification of the quartz and cristobalite polymorphs of crystalline silica upward to Group I, Carcinogenic to Humans.2 There is only limited evidence from animal studies that tridymite is carcinogenic, even though it is still a crystalline polymorph. In addition, exposure to inhaled silica can lead to diseases which do not involve the lungs.4 Employees exposed to silica have statistically significant increased rates of developing immunologic and autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus and sarcoidosis. Increased prevalence of renal disease, including end-stage renal failure, stomach and other cancers, has also been noted.
EXPOSURE CONTROL AND REGULATION
Exposure to crystalline silica can be controlled by the same methods as exposure to any other airborne dust. Engineering controls include ventilation, enclosure or isolation of the dustproducing activity. Silica-containing abrasives used in ‘‘sandblasting’’ can be replaced with less harmful alternatives. Job rotation and wet methods are administrative and work practice controls useful in minimizing dust exposure. Personal protective equipment, primarily respirators, is the final resort if engineering and work practice controls cannot reduce ambient concentrations to a safe level. Despite the known hazards and variety of health effects of exposure to crystalline silica, OSHA has no substance-specific standards as are provided for asbestos, lead, cadmium, and 22 other materials, in addition to 13 select carcinogens.11 None of these substances is found as widely as crystalline silica. Federal statutory control of crystalline silica is limited to compliance with the published permissible exposure limits (PELs). Meaningful control requires standards against which ambient expo-
Journal of Chemical Health & Safety, March/April 2010
sures can be measured. The current OSHA crystalline quartz PEL for the Construction industry12 is 250 mppcf : ð%SiO2 þ 5Þ mppcf : millions of particles per cubic foot of air; based on impinger samples counted by light-field techniques. Per a foot note to the table, ‘‘The percentage of crystalline silica in the formula is the amount determined from airborne samples, except in those instances in which other methods have been shown to be applicable.’’ The General Industry standards include a PEL for total quartz:13 ð30 mg=m3 Þ ð%SiO2 þ 2Þ The current PEL for respirable crystalline quartz for General Industry is either 250 mppcf ð10 mg=m3 Þ or ð%SiO2 þ 5Þ ð%SiO2 þ 2Þ The two PELS (mppcf and mg/m3) cannot be interconverted with mathematical exactitude. The actual measurement of crystalline silica exposure remains problematic because of the need to identify the proportion of crystalline silica in a sample. This information is necessary to calculate the PEL of a particular silica-containing material. The determination of actual silica content is crucial for regulatory compliance as well as health protection: Hazard Communication, for example, requires identification of crystalline silica at any level in excess of 0.1%.
ANALYTICAL METHODS
Determination of the percent silica content of a sample is not straightforward. While chemical tests for elemental silicon are readily available and accurate to the level of 0.1%, elemental analysis does not identify the form in which silicon is present. Methods of isolating the silica component may be less than satisfactory, because of incomplete separation or removal of some of the silica content along with the non-silica components.
7
Additionally, analytical methods may either change or fail to distinguish among the various polymorphs of silica. Analytical methods for crystalline silica may be either chemical, physical, or a combination of the two.14 Chemical methods typically cannot identify the specific polymorph present in a sample. Fusion of a sample with sodium pyrosulfate removes non-silica content, leaving an insoluble residue containing quartz, cristobalite, tridymite and opal.15 This method does not distinguish between the specific crystalline forms, or between crystalline silica and amorphous opal. Strong acids may be used to remove other components of a mixture or matrix, leaving behind the relatively insoluble crystalline silica. Unfortunately, some of the contaminant material may not dissolve unless digestion times are extended, even to several days. Such extended digestion may proceed to dissolve some of the crystalline silica present,16 especially if the particles are small. Rate of dissolution may also be modified by the presence of amorphous layers that may form on the crystalline surfaces. This loss of material is especially significant in mixtures where the crystalline silica is present in low concentrations. NIOSH has provided standard methods of analysis. NIOSH Method 7601,17 which relies on digestion in phosphoric acid, is primarily intended for characterization of respirable dusts, and is often used in industrial settings to determine quantatively the crystalline silica levels in samples that do not include amorphous silicas and other silicas which might be resistant to digestion. The method is used to concentrate samples before analysis by X-ray diffraction, such as NIOSH Method 7500.18 NIOSH 7500 is a nondestructive method and can identify individual crystalline silica polymorphs and even quantify the amount of quartz and cristobalite above threshold levels of 10 mg and 30 mg respectively. In any quantitative X-ray diffraction method, spectral overlap may complicate interpretation of the diffraction pattern,
8
and the technique is useful primarily when silica is a major phase. When the sample involves thicker films, the NIOSH absorption correction factor is ‘‘not always appropriate’’.14 NIOSH Method 760219 describes IR methods of identifying crystalline silica in bulk samples, and NIOSH 760320 refines the method when the sample is mixed with coal dust. Samples should be concentrated before analysis. Spectral overlap with other forms of silicates may confound analysis unless these materials are removed. It is also difficult to distinguish among polymorphs of crystalline silica using IR methods. Observation and identification of crystalline silica particles is possible using microscopic techniques. This is especially appropriate if the mppcf PEL is used. However, microscopic analysis is exceedingly time consuming and requires a highly skilled analyst.
CONCLUSIONS
6.
7.
8.
9.
10.
11.
Silicosis and other conditions related to exposure to crystalline silica have historically been significant public health and occupational health issues. Despite better control of exposures, the hazards still remain. Regulatory control of exposure is hampered by the lack of a specific standard, and is further complicated by the difficulty of accurately determining the crystalline silica content of samples used for exposure monitoring.
12. 13. 14.
15.
REFERENCES 1. Crystalline Silica Primer, US Dept of Interior, Special Publication, 1992. 2. IARC, Silica, Some Silicates, Coal Dust and para-Aramid Fibrils, vol. 68, Lyon, International Agency for Research on Cancer, 1997. 3. Rosen, G. The History of Miner’s Disease: A Medical and Social Interpretation; Schuman; NY, 1943, pp. 459–76. 4. PL 03-00-007 – National Emphasis Program – Crystalline Silica. Accessed on 7/13/2009 at http://www.osha.gov/ pls/oshaweb. 5. ‘‘Silicosis Mortality, Prevention and Control — United States, 1968–2002’’.
16.
17.
18.
19.
20.
Accessed on 8/2/2009 at http://www. cdc.gov/mmw r/preview/mmwrhtml/ mm5416a2.htm. ‘‘Hawks Nest worker graves lay forgotten for decades’’ from the Charleston Gazette, Charleston, WV, February 24, 2008. Quoted by the Greater Southeastern Massachusetts Labor Council. Accessed on 8/2/2009 at http://www. gsmlaborcouncil.org/node/2427. Peters, J. M. In J. A. Merchant (Ed.), Silicosis, Occupational Respiratory Diseases, Division of Respiratory Disease Studies, Appalachian Laboratory for Occupational Safety and Health. National Institute for Occupational Safety and Health, 1986. Westerholm, P. Silicosis observations on a case register. Scand. J. Work Environ. Health, 1980, 6(Suppl. 2), 1–86. Finkelstein, M.; Kusiak, R.; Suranyi, G. Mortaility among miners receiving workmen’s compensation for silicosis in Ontario: 1940–1975. J. Occup. Med. 1982, 24, 663–667. IARC, Supplement 7 of IARC Monographs. Lyon, International Agency for Research on Cancer, vol. 42, 1987. 29 CFR 1910.1001-1018; 29 CFR 1910.1025-1029, 29 CFR 1919.10431050. 29 CFR 1926.55, Appendix A, mineral dusts. 29 CFR 1910.1000, Table Z-3: mineral dusts. Miles William, J. Issues and controversy: the measurement of crystalline silica; Review papers on analytical methods. AIHA J. 1999, 60(May– June), 396–402. Chapman, S. L.; Syers, J. K.; Jackson:, M. L. Quantatitive determination of quartz in soils, sediemtns and rocks by pyrosulfate fusion and hydorfluosilicic acid treatment. Soil Sci. 1969, 107, 348–355. Knopf, A. The Quantitative Determination of Quartz (free silica) in dusts. US Public Health Report, No. 48, Washington, DC. 1933, pp. 183–90. NIOSH 7601. Accessed on 8/18/09 at http://www.cdc.gov/niosh/nmam/ pdfs/7601.pdf. NIOSH 7500. Accessed on 8/18/09 at http://www.cdc.gov/niosh/nmam/ pdfs/7500.pdf. NIOSH 7602. Accessed on 8/18/09 at http://www.cdc.gov/niosh/nmam/ pdfs/7602.pdf. NIOSH 7603. Accessed on 8/18/09 at http://www.cdc.gov/niosh/nmam/ pdfs/7603.pdf.
Journal of Chemical Health & Safety, March/April 2010
A brief overview of crystalline silica Silicon, and its oxide silica, are naturally abundant. Exposure to crystalline silica has long been known to cause silicosis and other lung disorders. Crystalline silica exposures are also associated with development of active tuberculosis, lung cancer, and certain autoimmune and renal disorders. Silicosis may occur in acute, accelerated and chronic forms with latency periods ranging from weeks to 40+ years, respectively. Silica exposure is controlled by the same methods that apply to any other dust inhalation hazard. No specific OSHA standard applies, beyond the PELs published in 29 CFR. These PELs depend on determination of the percent silica in a sample. This analysis should be performed in accordance with NIOSH analytical methods.
By Eileen Mason, Sophie K. Thompson
INTRODUCTION
Silicon is the second-most abundant element in the world.1 Silica, the common oxide, (SiO2) occurs naturally and is widespread. Crystalline forms of silica include alpha- and beta-quartz, cristobalite and tridymite. Because, alphaquartz is the most thermodynamically stable form, most naturally occurring crystalline silica is found in this morphology.2 Alpha-quartz has the greatest health impact because it is encountered most often. Cristobalite and tridymite are formed by exposure to high temperature, such as volcanic processes, or by calcining diatomaceous earth. Tridymite tends to be less hazardous than other crystalline forms, and amorphous silica is of lesser toxicological interest than crystalline silica. Because silica, especially in the form of quartz, is so ubiquitous, exposures may occur in any dusty location, and Eileen Mason is affiliated with Murray State University, Occupational Safety & Health, 157 IT Center, Murray, KY 420071, United States (e-mail: [email protected]). Sophie K. Thompson is affiliated with Old Dominion University, United States (e-mail: [email protected]).
6
may be both occupational and nonoccupational. Common beach sand is almost pure silica, as is volcanic glass. Topsoil, dust, and sedimentary and metamorphic rocks all contain silica in varying amounts. Granites contain in the neighborhood of 30% quartz, while shales are comprised of about 20% quartz. Some igneous rock may contain silica. Diatoms and radiolarians extract silica from water to form shells. Deposits of these shells are mined as diatomaceous earth, a noncrystalline form of silica. Opal, perlite and pumice are composed of amorphous hydrated silica. Historical Background
Reports of adverse health effects of exposure to silica date back to the ancient Greeks.3 Agricola’s 1556 Treatise on Mining describes pulmonary effects of silica exposure, and the topic is again discussed by Ramazzini in 1713. Today, we realize that it is primarily the crystalline form of silica that presents the health hazard. Such information was not available historically. Silicosis, a type of pneumoconiosis, occurs when crystalline silica particles are deposited in the lung tissue, leading to fibrotic changes. This accumulation of crystalline silica dust in the lungs has been known historically as ‘‘miners’ asthma’’, ‘‘potters rot’’, ‘‘phthisis’’, ‘‘stonemason’s disease’’ and ‘‘sewer disease’’.4 By the 1920s, dust inhalation, especially in the granite industry, was recognized as a serious health problem.
ß Division of Chemical Health and Safety of the American Chemical Society Elsevier Inc. All rights reserved.
During the 1930s, after the Hawks Nest disaster gained national attention, silicosis was considered the most serious occupational disease in this country. The Hawks Nest disaster occurred during the period 1930– 1931, when approximately 5,000 workers were employed to bore a tunnel through Gauley Mountain in West Virginia.5 About half of these employees worked inside the tunnel, excavating sandstone which was estimated to contain over 90% silica. Respiratory protection was supplied only to management, and wet drilling methods were used infrequently, since dry drilling was faster. A historical marker on the site documents a total of 109 deaths, but subsequent studies determined that at least 764 workers died due to silicosis and other silica-related conditions. At this time, safety laws were promulgated at the state level. Although only 11 states regulated silica exposure prior to Hawks Nest, congressional hearings held in 1937 were followed by passage of laws in an additional 35 states.
TOXICOLOGY
Silicosis may be acute, chronic, or accelerated. In all its forms, silicosis is incurable and symptoms are difficult to manage. The disease may progress even if there is no further exposure to silica. Inevitably, silicosis leads to serious loss of function and often death.
1871-5532/$36.00 doi:10.1016/j.jchas.2009.09.001
Overwhelming exposure to silica results in acute silicosis. Symptoms may become apparent within a few weeks. Employees at the Hawks Nest project were hired for periods averaging only 15 weeks – so that they could ‘‘leave the area and die someplace far from the source of their illness’’.6 Although relatively rare, acute silicosis still occurs among sandblasters and silica flour mill employees.7 Acute silicosis seems to involve an immune mechanism distinct from those associated with chronic and accelerated silicosis. Chronic silicosis, also known as silico-proteinosis or alveolar lipoproteinosis-like silicosis, is the most common presentation and typically appears 20– 40 years after initial exposure. Symptoms may be mild or absent for extended periods, with subsequent development of a dry cough and shortness of breath during exertion. Eventually, the cough becomes persistent and productive, with shortness of breath during normal activity. Examination of chest X-rays shows development of characteristic, extremely hard silica nodules, primarily located in the mid- and upper zones of the lung. These nodules proliferate and may coalesce as the disease progresses to massive pulmonary fibrosis. Eventually, pneumothorax and respiratory failure result. Accelerated silicosis is similar to chronic silicosis, but the latency period is reduced to 5–15 years from initial exposure, and the disease progresses more rapidly than does chronic silicosis. Exposure to crystalline silica is associated with a variety of respiratory diseases in addition to silicosis. There is a clear association between silica exposure and development of active tuberculosis, not only among silicotic individuals, but even in those who have long-term exposure to silica dust but do not have silicosis. Epidemiological studies have also shown an association between silica exposure and chronic bronchitis, emphysema and other forms of chronic obstructive pulmonary disease. Initial reports from Sweden8 and Ontario9 and additional studies during the 1980s confirmed a probable relationship between crystalline silica and
lung cancer. In 1987, IARC classified crystalline silica as Group 2A, Probably Carcinogenic to Humans.10 In 1996, with additional information, IARC revised the classification of the quartz and cristobalite polymorphs of crystalline silica upward to Group I, Carcinogenic to Humans.2 There is only limited evidence from animal studies that tridymite is carcinogenic, even though it is still a crystalline polymorph. In addition, exposure to inhaled silica can lead to diseases which do not involve the lungs.4 Employees exposed to silica have statistically significant increased rates of developing immunologic and autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus and sarcoidosis. Increased prevalence of renal disease, including end-stage renal failure, stomach and other cancers, has also been noted.
EXPOSURE CONTROL AND REGULATION
Exposure to crystalline silica can be controlled by the same methods as exposure to any other airborne dust. Engineering controls include ventilation, enclosure or isolation of the dustproducing activity. Silica-containing abrasives used in ‘‘sandblasting’’ can be replaced with less harmful alternatives. Job rotation and wet methods are administrative and work practice controls useful in minimizing dust exposure. Personal protective equipment, primarily respirators, is the final resort if engineering and work practice controls cannot reduce ambient concentrations to a safe level. Despite the known hazards and variety of health effects of exposure to crystalline silica, OSHA has no substance-specific standards as are provided for asbestos, lead, cadmium, and 22 other materials, in addition to 13 select carcinogens.11 None of these substances is found as widely as crystalline silica. Federal statutory control of crystalline silica is limited to compliance with the published permissible exposure limits (PELs). Meaningful control requires standards against which ambient expo-
Journal of Chemical Health & Safety, March/April 2010
sures can be measured. The current OSHA crystalline quartz PEL for the Construction industry12 is 250 mppcf : ð%SiO2 þ 5Þ mppcf : millions of particles per cubic foot of air; based on impinger samples counted by light-field techniques. Per a foot note to the table, ‘‘The percentage of crystalline silica in the formula is the amount determined from airborne samples, except in those instances in which other methods have been shown to be applicable.’’ The General Industry standards include a PEL for total quartz:13 ð30 mg=m3 Þ ð%SiO2 þ 2Þ The current PEL for respirable crystalline quartz for General Industry is either 250 mppcf ð10 mg=m3 Þ or ð%SiO2 þ 5Þ ð%SiO2 þ 2Þ The two PELS (mppcf and mg/m3) cannot be interconverted with mathematical exactitude. The actual measurement of crystalline silica exposure remains problematic because of the need to identify the proportion of crystalline silica in a sample. This information is necessary to calculate the PEL of a particular silica-containing material. The determination of actual silica content is crucial for regulatory compliance as well as health protection: Hazard Communication, for example, requires identification of crystalline silica at any level in excess of 0.1%.
ANALYTICAL METHODS
Determination of the percent silica content of a sample is not straightforward. While chemical tests for elemental silicon are readily available and accurate to the level of 0.1%, elemental analysis does not identify the form in which silicon is present. Methods of isolating the silica component may be less than satisfactory, because of incomplete separation or removal of some of the silica content along with the non-silica components.
7
Additionally, analytical methods may either change or fail to distinguish among the various polymorphs of silica. Analytical methods for crystalline silica may be either chemical, physical, or a combination of the two.14 Chemical methods typically cannot identify the specific polymorph present in a sample. Fusion of a sample with sodium pyrosulfate removes non-silica content, leaving an insoluble residue containing quartz, cristobalite, tridymite and opal.15 This method does not distinguish between the specific crystalline forms, or between crystalline silica and amorphous opal. Strong acids may be used to remove other components of a mixture or matrix, leaving behind the relatively insoluble crystalline silica. Unfortunately, some of the contaminant material may not dissolve unless digestion times are extended, even to several days. Such extended digestion may proceed to dissolve some of the crystalline silica present,16 especially if the particles are small. Rate of dissolution may also be modified by the presence of amorphous layers that may form on the crystalline surfaces. This loss of material is especially significant in mixtures where the crystalline silica is present in low concentrations. NIOSH has provided standard methods of analysis. NIOSH Method 7601,17 which relies on digestion in phosphoric acid, is primarily intended for characterization of respirable dusts, and is often used in industrial settings to determine quantatively the crystalline silica levels in samples that do not include amorphous silicas and other silicas which might be resistant to digestion. The method is used to concentrate samples before analysis by X-ray diffraction, such as NIOSH Method 7500.18 NIOSH 7500 is a nondestructive method and can identify individual crystalline silica polymorphs and even quantify the amount of quartz and cristobalite above threshold levels of 10 mg and 30 mg respectively. In any quantitative X-ray diffraction method, spectral overlap may complicate interpretation of the diffraction pattern,
8
and the technique is useful primarily when silica is a major phase. When the sample involves thicker films, the NIOSH absorption correction factor is ‘‘not always appropriate’’.14 NIOSH Method 760219 describes IR methods of identifying crystalline silica in bulk samples, and NIOSH 760320 refines the method when the sample is mixed with coal dust. Samples should be concentrated before analysis. Spectral overlap with other forms of silicates may confound analysis unless these materials are removed. It is also difficult to distinguish among polymorphs of crystalline silica using IR methods. Observation and identification of crystalline silica particles is possible using microscopic techniques. This is especially appropriate if the mppcf PEL is used. However, microscopic analysis is exceedingly time consuming and requires a highly skilled analyst.
CONCLUSIONS
6.
7.
8.
9.
10.
11.
Silicosis and other conditions related to exposure to crystalline silica have historically been significant public health and occupational health issues. Despite better control of exposures, the hazards still remain. Regulatory control of exposure is hampered by the lack of a specific standard, and is further complicated by the difficulty of accurately determining the crystalline silica content of samples used for exposure monitoring.
12. 13. 14.
15.
REFERENCES 1. Crystalline Silica Primer, US Dept of Interior, Special Publication, 1992. 2. IARC, Silica, Some Silicates, Coal Dust and para-Aramid Fibrils, vol. 68, Lyon, International Agency for Research on Cancer, 1997. 3. Rosen, G. The History of Miner’s Disease: A Medical and Social Interpretation; Schuman; NY, 1943, pp. 459–76. 4. PL 03-00-007 – National Emphasis Program – Crystalline Silica. Accessed on 7/13/2009 at http://www.osha.gov/ pls/oshaweb. 5. ‘‘Silicosis Mortality, Prevention and Control — United States, 1968–2002’’.
16.
17.
18.
19.
20.
Accessed on 8/2/2009 at http://www. cdc.gov/mmw r/preview/mmwrhtml/ mm5416a2.htm. ‘‘Hawks Nest worker graves lay forgotten for decades’’ from the Charleston Gazette, Charleston, WV, February 24, 2008. Quoted by the Greater Southeastern Massachusetts Labor Council. Accessed on 8/2/2009 at http://www. gsmlaborcouncil.org/node/2427. Peters, J. M. In J. A. Merchant (Ed.), Silicosis, Occupational Respiratory Diseases, Division of Respiratory Disease Studies, Appalachian Laboratory for Occupational Safety and Health. National Institute for Occupational Safety and Health, 1986. Westerholm, P. Silicosis observations on a case register. Scand. J. Work Environ. Health, 1980, 6(Suppl. 2), 1–86. Finkelstein, M.; Kusiak, R.; Suranyi, G. Mortaility among miners receiving workmen’s compensation for silicosis in Ontario: 1940–1975. J. Occup. Med. 1982, 24, 663–667. IARC, Supplement 7 of IARC Monographs. Lyon, International Agency for Research on Cancer, vol. 42, 1987. 29 CFR 1910.1001-1018; 29 CFR 1910.1025-1029, 29 CFR 1919.10431050. 29 CFR 1926.55, Appendix A, mineral dusts. 29 CFR 1910.1000, Table Z-3: mineral dusts. Miles William, J. Issues and controversy: the measurement of crystalline silica; Review papers on analytical methods. AIHA J. 1999, 60(May– June), 396–402. Chapman, S. L.; Syers, J. K.; Jackson:, M. L. Quantatitive determination of quartz in soils, sediemtns and rocks by pyrosulfate fusion and hydorfluosilicic acid treatment. Soil Sci. 1969, 107, 348–355. Knopf, A. The Quantitative Determination of Quartz (free silica) in dusts. US Public Health Report, No. 48, Washington, DC. 1933, pp. 183–90. NIOSH 7601. Accessed on 8/18/09 at http://www.cdc.gov/niosh/nmam/ pdfs/7601.pdf. NIOSH 7500. Accessed on 8/18/09 at http://www.cdc.gov/niosh/nmam/ pdfs/7500.pdf. NIOSH 7602. Accessed on 8/18/09 at http://www.cdc.gov/niosh/nmam/ pdfs/7602.pdf. NIOSH 7603. Accessed on 8/18/09 at http://www.cdc.gov/niosh/nmam/ pdfs/7603.pdf.
Journal of Chemical Health & Safety, March/April 2010